CAMPYLOBACTER-PYLORI - ASSOCIATIONS WITH ANTRAL AND FUNDIC MUCOSAL HISTOLOGY AND DIAGNOSIS BY SEROLOGY IN PATIENTS WITH UPPER GASTROINTESTINAL SYMPTOMS

  • 1 April 1989
    • journal article
    • research article
    • Vol. 84 (4), 367-371
Abstract
We obtained a sample of serum and mucosal biopsies from the antrum and usually from the corpus of the stomach from 35 symptomatic patients during routine endoscopy to analyze for the relationship between Campylobacter pylori infection, inflammation, and the diagnostic utility of a C. pylori IgG antibody assay. C. pylori was identified prospectively by culture and/or silver stain in gastric biopsies from 24 patients, and the antibody was detected in 19 (79%) of these patients. The antibody assay was positive in three other patients, two of whom had C. pylori, on reexamination of their biopsies. The accuracy of the antibody assay was 83%. Inflammation was detected in all C. pylori-positive antral biopsies (N = 19). However, five (71%) of seven antral biopsies from patients in whom all tests were C. pylori negative, also had inflammation, constituting 17% of all patients with antral gastritis (N = 30). Both antral and fundic mucosa were obtained from 26 patients and, in this group, C. pylori was detected in fundic mucosa from all patients in whom the organism also was present in the antrum (N = 15). In significant (p < 0.001) contrast to C. pylori-positive antral histology, fundic mucosal histology was normal in 6 (40%) of 15 C. pylori-positive biopsies, all from patients with peptic ulcer disease. We concluded that C. pylori antibody assays will be useful for epidemiological studies and initial screening of the C. pylori status of individual patients. In addition, there is a high concordance rate between antral and fundic mucosa for the prevalence of C. pylori, but in contrast to the probable etiological role of C. pylori in antral gastritis, the organism appears to be only a commensal of fundic mucosa. Moreover, C. pylori infection is not evident in all patients with type B gastritis.